Information is transmitted along the axon’s length which can be between less than
a 1,000th of a centimetre or a metre long, depending on its function. It is filled
with jelly-like axoplasm and most neurons in the brain are wrapped in Schwann cells
which form a fatty myelin sheath around the axon. The myelin sheath insulates neurons
from each other so that the electrical impulse travelling along one neuron will not
affect its neighbours. It also speeds up information via the Schwann cells. The impulse
being transmitted jumps from one gap to another in the myelin sheath - the Nodes
of Ranvier.
There are 3 types of neurons:-
- Afferent (sensory) neurons - carry information about external stimuli - eg: light
or touch - from sensory receptors to the central nervous system (CNS)
- Efferent (motor) neurons - carry information from the CNS to muscles and glands
- Interneurons (connector neurons) - transmit information to other neurons and are
only found in the CNS
No 2 neurons of any type are identical - though the cellular structures are similar.
When an axon is at rest, sodium ions - tiny, electrically-charged particles of sodium
- are pumped out of the axon and potassium ions are pumped in. When an impulse passes
along the axon, sodium ions rush in and this causes action potential, an electrical
charge, to pass along the neuron. However, action potential will only be produced
if the stimulus to the neuron is strong enough - ie: it reaches threshold level.
The strength of the stimulus is determined by its frequency.
Transmission between neurons
The tiny synaptic gap (or synaptic cleft) is between an axon terminal button (or
synaptic knob) and the dendrites of the next neuron. The dendrites contain receptor
molecules of a certain shape prepared to receive the neurotransmitters (chemical
messengers) from the synaptic vesicles of the first neuron’s terminal button. The
receptor molecules are like locks: if the neurotransmitter fits the receptor molecule,
the message is passed on; if it doesn’t, the message is blocked.
In this way, synapses can be excitatory or inhibitory. With some neurons having upto
10,000 synapses - an efferent neuron in the spinal cord will have over 1,000 dendrites
- inhibitory synapses are vital to ensure the spread of electrical impulses is kept
channelled within the correct circuits and not allowed to spread through other neural
networks.
When the impulse arrives at the terminal button, it makes the pre-synaptic membrane
more permeable to calcium ions in the synaptic gap. These flow into the button and
cause the vesicles to fuse with the pre-synaptic membrane and
discharge their neurotransmitters into the cleft. The calcium ions, having done their
job, are pumped out of the terminal button.
The neurotransmitters diffuse across the cleft and attach to the receptor molecules
on the post-synaptic membrane of the receiving dendrite. This allows sodium ions
in the synaptic gap to diffuse through the post-synaptic membrane, passing on the
impulse if the threshold is reached to trigger action potential.
The neurotransmitter substance, having served its purpose, is broken down by enzymes.
Its constituent parts are reabsorbed by the pre-synaptic membrane of the first neuron
and made back into neurotransmitter substance in the vesicles - after which the synapse
is ready to receive another impulse.
As a general rule, each neuron contains only one neurotransmitter.
Some key neurotransmitters
Acetylcholine (ACh) was the first neurotransmitter to be identified some 70 years
ago. This chemical is released by neurons connected to voluntary muscles (causing
them to contract) and by neurons that control the heartbeat. ACh also serves as a
transmitter in many regions of the brain.
Antibodies that block the receptor molecules for ACh cause Myasthenia Gravis, a disease
characterised by fatigue and muscle weakness.
Recent discoveries suggest ACh may be critical for normal attention, memory and sleep.
In REM sleep the activity of ACh in specific parts of the body is blocked, resulting
in the paralysis which prevents us acting out our dreams. (‘REM Sleep Behaviour Disorder’
is caused by the failure of the magnocellular nucleus in the brain to send a signal
via the spinal cord to block Ach enabling motor neurons to become activated - with
the result that the sufferer does act out their dreams!) Since ACh-releasing neurons
die in Alzheimer’s Disease patients, finding ways to restore this neurotransmitter
is one goal of current research.
The catecholamines dopamine and noradrenaline are widely present in the brain and
peripheral nervous system. Dopamine, which is present in 3 circuits in the brain,
controls movement, is strongly linked to psychiatric symptoms such as psychosis and
regulates hormonal responses.
The dopamine circuit that regulates movement has been directly related to disease.
The brains of people with Parkinson’s Disease - with symptoms of muscle tremors,
rigidity and difficulty in moving - have practically no dopamine. Thus, medical scientists
found that the administration of Levodopa, a substance from which dopamine is synthesized,
is an effective treatment for Parkinson’s, allowing patients to walk and perform
skilled movements successfully.
Another dopamine circuit is thought to be important for cognition and emotion; abnormalities
in this system have been implicated in Schizophrenia. Because drugs that block dopamine
receptors in the brain are helpful in diminishing psychotic symptoms, learning more
about dopamine is important to understanding mental illness. Researchers such as
A J Giannini (1987) have implicated the high levels of dopamine stimulated in the
mesolimbic pathway by addictive substances ranging from coffee to cocaine as being
a key factor in bringing about addiction.
In a third circuit, dopamine regulates the endocrine system. It directs the hypothalamus
to manufacture hormones and hold them in the pituitary gland for release into the
bloodstream, or to trigger the release of hormones held within cells in the pituitary.
Nerve fibers containing noradrenaline are present throughout the brain. Deficiencies
in this neurotransmitter occur in patients with Alzheimer’s Disease, Parkinson’s
Disease and those with Korsakoff’s Syndrome, a cognitive disorder associated with
chronic alcoholism. Thus, researchers believe noradrenaline may play
a role in both learning and memory. Noradranaline also is secreted by the sympathetic
nervous system in the periphery to regulate heart rate and blood pressure. Acute
stress increases the release of noradrenaline.
Serotonin is present in many tissues, particularly blood platelets and the lining
of the digestive tract and the brain. Serotonin was first thought to be involved
in
high blood pressure because it is present in blood and induces a very powerful contraction
of smooth muscles. In the brain, it has been implicated in sleep, mood, Depression
and anxiety.
Because serotonin is thought to control the different switches affecting various
emotional states, neuroscientists think these switches can be manipulated by analogs,
chemicals with molecular structures similar to serotonin. Drugs that alter serotonin’s
action, such as Fluoxetine (Prozac), have relieved symptoms of Depression and
Obsessive-Compulsive Disorder.
The neurotransmitters glutamate and aspartate act as excitatory signals. Glycine
and gamma-aminobutyric acid (GABA) inhibit the firing of neurons. The activity of
GABA is increased by Benzodiazepine (Valium) and by anticonvulsant drugs. In Huntington’s
Disease, a hereditary disorder that begins during mid-life, the GABA-producing neurons
in the brain centres coordinating movement degenerate, thereby causing incontrollable
movements.
Glutamate or aspartate activate N-methyl-D-aspartate (NMDA) receptors, which have
been implicated in activities ranging from learning and memory to development and
specification of nerve contacts in a developing animal. The stimulation of NMDA receptors
may promote beneficial changes in the brain, whereas overstimulation can cause nerve
cell damage or cell death in trauma and stroke. Key questions remain about this receptor’s
precise structure, regulation, location and function.
In 2004 Daniel Javitt & Joseph Coyle identified fluctuations in glutamate in different
parts of the brain as a second neurotransmitter linked to various schizophrenic symptoms
(dopamine being the first) - see The Schizophrenic Brain.
